Vancomycin-resistant enterococci (VRE) are becoming increasingly prevalent isolates in microbiology laboratories, and are posing a major infectious disease problem particularly in intensive care units. Resistance is conferred by modification of peptidoglycan precursors and, in E. faecium and E. faecalis, is conferred by the presence of either the vanA or vanB genes. The VanA resistance phenotype is characterized by high-level, inducible, resistance to both vancomycin and teicoplanin (another glycopeptide antibiotic), while vanB typically only confers resistance to vancomycin. Case reports have documented the development of teicoplanin resistance in vivo in a vanB isolate, questioning the utility of teicoplanin as a treatment modality for infection with VRE. These studies have also shown that development of teicoplanin resistance in these organisms was associated with constitutive expression of the vanB gene product. We have obtained similar VRE isolates, and intend to investigate the regulation of vanB expression in both the wild-type and teicoplanin resistant organisms. We hope that such an investigation will provide important information about both the underlying genetic control of vancomycin resistance in enterococci, and the more fundamental question of gene regulation in this group of important human pathogens.